Pathophysiology of delirium

TLDR: Postoperative cognitive changes are more common in older than in younger patients, and they can be categorized as postoperative delirium, postoperative cognitive dysfunction and dementia, and the mechanisms responsible are not fully understood, but it is certain that they are multifactorial.

Abstract: Today's understanding of the pathophysiological mechanisms of delirium is still limited, but there are several promising hypotheses. It is believed that biomarkers sensitive to death of neurons or glial cells indicate delirium. Several neurotransmitters are considered to be involved in the state of delirium, with greatest emphasis on acetylcholine and dopamine acting in opposite ways; acetylcholine reduces, while dopamine increases neuron excitability. Other neurotransmitters that probably play a role in the pathogenesis of delirium are GABA, glutamate and monoamines. Sepsis leading to systemic inflammatory response syndrome often presents with delirium and perhaps is the most common causal factor for delirium in intensive care unit; sedatives and analgesics are also common iatrogenic risk factors. Patients receiving benzodiazepines are more likely to have postoperative delirium than those who do not. Postoperative cognitive changes are more common in older than in younger patients, and they can be categorized as postoperative delirium, postoperative cognitive dysfunction and dementia. The mechanisms responsible for postoperative cognitive changes are not fully understood, but it is certain that they are multifactorial. Risk factors may be associated with patient characteristics, type of surgery and type of anesthesia.